Reduction of endothelial microparticles in active SLE suppresses inflammatory response

  In this prospective observational study, we looked at whether patients with active systemic lupus erythematosus (SLE) had higher indices of vascular endothelial damage and dysfunction than healthy controls, and to see whether improved disease control was associated with these indices.  Twenty-seven patients with active SLE (4 or more meeting American College of Rheumatology (ACR) criteria) and 22 age-matched controls were evaluated. Endothelial microparticles (EMPs; CD31+/membrane-linked protein V+/CD42b) were measured by flow cytometry. Brachial artery diastolic function (FMD) was measured with automated software. A secondary evaluation was performed in 22 patients after 20 weeks (16, 22) of new immunosuppressive therapy.  The activity assessment score according to (BILAG-2004) for patients with SLE was 14 (12, 22). Endothelial granule CD31+ /membrane coupling protein V+/CD42b was elevated in SLE patients compared to controls [157548/ml (59,906, 272643) vs 41025 (30179, 98082), p=0.003 ] and endothelium-dependent brachial artery diastolic function was decreased [1.63% (-1.22, 5.32) vs 5.40% (3.02, 8.57), p=0.05]. Endothelial granule CD31+/membrane-linked protein V+/CD42b was negatively correlated with brachial artery diastolic function (%) (r20.40, p=0.006). At follow-up, after a secondary assessment after treatment, the patient activity assessment score according to (BILAG-2004) was a change of -11 (-18, -3). Endothelial granule CD31+/membrane association protein V+/CD42b levels were decreased [166982/ml (59906, 278775 vs 55655 (29475, 188 659), p=0.02] and brachial artery diastolic function was improved [0.33% (2.31, 4.1) vs 3.19% (0.98, 5.09), p= 0.1].  There is evidence that SLE activity is associated with endothelial damage and endothelial dysfunction and that suppression of the inflammatory response is beneficial for disease improvement. Better control of inflammatory disease activity may improve the risk of cardiovascular disease in patients with SLE.